Proteinuria is only discovered when patients check their urine, and we usually cannot detect it ourselves. Don't simply assume that proteinuria is excreted from the body, as it can actually cause great harm to the body.
Proteinuria poses many hazards to the human body. The occurrence of proteinuria is not only due to a large loss of nutritional protein, but also causes damage to the glomerulus, renal tubules, and other organs, leading to renal fibrosis and various kidney diseases. Research has confirmed that the occurrence of proteinuria is the first independent risk factor for uremia, and the greatest harm of proteinuria lies in its toxic effect on the kidneys, leading to uremia. So what are the specific hazards of proteinuria?
(1) Mesangial toxicity of proteinuria:
In the model of renal failure, the accumulation of serum proteins in the glomerular mesangium can be observed. The aggregation of these macromolecular substances in the mesangial area can cause damage to mesangial cells, increase the synthesis of various mesangial matrices, and thus lead to glomerulosclerosis. In a proteinuria nephropathy model, the accumulation of low density lipoprotein (LDL) and extremely low density lipoprotein (VLDL) apolipoprotein B and apolipoprotein A in the glomerulus can ultimately lead to glomerulosclerosis.
(2) The toxic effect of proteinuria on proximal tubular cells:
When proteinuria occurs, the amount of protein entering the epithelial cells of renal tubules increases, leading to an increase in lysosomal activity. This suggests that the protein causes lysosomal leakage into the cytoplasm of tubular cells, and subsequent cell damage can stimulate inflammation and scar formation.
(3) Biological changes in tubular cells caused by proteinuria:
Many kidney diseases with proteinuria exhibit excessive cell proliferation, representing a non adaptive response that leads to kidney failure. More and more evidence suggests that proteins can directly regulate the function of tubular cells, alter their growth characteristics, cytokine and matrix protein phenotype expression, and lead to the release of PDGF, FN, and MCP-1 from the basal side of the tubules, inducing the process of fibrosis.
(4) Increased interstitial hypoxia caused by proteinuria:
Protein urine reabsorption requires extra energy to digest a large amount of protein, which can cause hypoxia of tubular cells, leading to tubular cell damage.
If there are transient symptoms of proteinuria, it has little impact on the body. If proteinuria symptoms occur frequently, it is more harmful to the kidneys.